The cancer drug vemurafenib has potent off-target effects on JNK signaling that contribute to the development of squamous cell carcinomas in humans and in mice.
Senescent cells contribute to age-related fat dysfunction and can directly impair healthy fat progenitor function, in part, via the secretion of activin A.
A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.
Dual FAK/PYK2 kinase inhibition disrupts GSK3β phosphorylation and may present a new treatment for colorectal cancer in patients carrying APC mutations.
Genomic gains in ovarian cancer can promote cisplatin resistance via a FAK, Wnt/beta-catenin and Myc signaling pathway supporting pluripotency genes and tumorspheres that can acquire FAK dependence for survival.
Integrin and actin associated proteins are resolved into four layers within myofibril attachments, an architecture requiring balanced positive and negative regulation of integrin adhesion with integrated mechanotransduction and actin pathways.
p27Kip1 directly controls invadopodia turnover by promoting the interaction of PAK1 with Cortactin, which induces Cortactin phosphorylation, invadopodia disassembly and facilitates invasion through extracellular matrix.
In keratinocytes, the BRAF and RAF1 proteins work independently to balance the activity of mitogenic and stress kinase cascades and uphold the mechanical and immunological barrier functions of the epidermis.
Disrupting extrusion, a process that drives epithelial cell death, leads to increased cell survival, poor barrier function, and enhanced cell invasion and, thereby, promotes tumor initiation and progression.
